Protection of retinal cells from ischemia by a novel gap junction inhibitor

Biochem Biophys Res Commun. 2008 Sep 5;373(4):504-8. doi: 10.1016/j.bbrc.2008.06.069. Epub 2008 Jun 30.

Abstract

Retinal cells which become ischemic will pass apoptotic signal to adjacent cells, resulting in the spread of damage. This occurs through open gap junctions. A class of novel drugs, based on primaquine (PQ), was tested for binding to connexin 43 using simulated docking studies. A novel drug has been synthesized and tested for inhibition of gap junction activity using R28 neuro-retinal cells in culture. Four drugs were initially compared to mefloquine, a known gap junction inhibitor. The drug with optimal inhibitory activity, PQ1, was tested for inhibition and was found to inhibit dye transfer by 70% at 10 microM. Retinal ischemia was produced in R28 cells using cobalt chloride as a chemical agent. This resulted in activation of caspase-3 which was prevented by PQ1, the gap junction inhibitor. Results demonstrate that novel gap junction inhibitors may provide a means to prevent retinal damage during ischemia.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Line
  • Cobalt / antagonists & inhibitors
  • Cobalt / toxicity
  • Gap Junctions / drug effects*
  • Ischemia / chemically induced
  • Ischemia / pathology
  • Ischemia / prevention & control*
  • Mefloquine / chemistry
  • Mefloquine / pharmacology
  • Primaquine / analogs & derivatives*
  • Primaquine / chemical synthesis
  • Primaquine / chemistry
  • Primaquine / pharmacology
  • Rats
  • Retina / drug effects*
  • Retina / pathology
  • Retinal Vessels / drug effects*

Substances

  • Cobalt
  • cobaltous chloride
  • Primaquine
  • Mefloquine